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At least 217 records · Page 12Linked to original sources
PubMed1985

[Baroreceptor reflexes after exposure to the hypotensive action of prazosin blocking postsynaptic alpha 1-adrenergic receptors].

The effect of prazosin, a selective blocker of post-synaptic alpha 1-adrenergic receptors, on baroceptor regulation was studied in experiments on narcotized rabbits. Following the intravenous administration of prazosin (5, 10 and 50 micrograms/kg) the blood pressure decreased, depending on the drug dosage. Transmission of the vasomotor activity to the vascular musculature was disrupted only partially. The pressor and depressor responses to changes in the output value of the baroreflex remained intact. The reaction of cardiac rhythm slowing in response to an increased pressure in the aorta disappeared. The sensitivity of the baroceptors was considerably elevated. In addition to the effector structures, prazosin influenced many other components of the system of the blood circulation reflex regulation.

Animals↗
PubMedDate not supplied

Effects of buflomedil on spontaneous vasomotion and mean arteriolar internal diameter in the hamster cheek pouch.

Intravital microscopy of the hamster cheek pouch microvasculature was used for in vivo studies on the effects of buflomedil, phentolamine (alpha-adrenergic receptor antagonist) and norepinephrine on the mean internal arteriolar diameter and spontaneous vasomotion. All drugs were applied topically. The vasomotor activity was studied in 125 arterioles (internal diameter range 18.0-62.0 microns) of 34 preparations. Addition of buflomedil (10(-9) to 10(-5) M) did not affect the arteriolar diameter significantly (from 100.7 +/- 3.5 to 106.4 +/- 1.8%, values expressed in percent of the initial diameter as mean +/- SE), but increased the vasomotion frequency and amplitude by approximately 20% (from 7.5 +/- 0.3 to 9.2 +/- 0.2 cpm) and 30% (from 7.3 +/- 0.3 to 10.0 +/- 0.5 micron), respectively. Phentolamine (10(-9) to 10(-5) M) dose-dependently increased the microvascular diameter (from 102.3 +/- 1.2 to 139.1 +/- 4.3%) and reduced the vasomotion frequency and amplitude (from 8.0 +/- 0.3 to 1.9 +/- 0.5 cpm and from 9.0 +/- 2.1 to 3.1 +/- 0.2 microns, respectively). Addition of buflomedil (10(-7) M) reduced the vasodilation evoked by phentolamine (from 103.3 +/- 0.7 to 127.0 +/- 1.5%) and potentiated its depressive effect on vasomotion frequency and amplitude (from 7.6 +/- 0.1 to 1.0 +/- 0.3 cpm and from 9.0 +/- 0.3 to 1.9 +/- 0.6 microns, respectively). Norepinephrine (10(-9) to 10(-5) M) dose-dependently decreased to arteriolar diameter (from 102.3 +/- 0.7 to 69.6 +/- 1.6%) and the vasomotion frequency and amplitude (from 8.4 +/- 0.2 to 0.4 +/- 0.3 cmp and from 8.7 +/- 0.2 to 0.5 +/- 0.4 microns, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Topical↗
PubMed2006

Hepatitis associated with low-dose venlafaxine for postmenopausal vasomotor symptoms.

OBJECTIVE: To report a case of drug-induced hepatitis associated with low-dose venlafaxine. CASE SUMMARY: A 60-year-old white woman receiving venlafaxine 75 mg daily for vasomotor symptoms presented after one month of therapy with nonspecific complaints, including abdominal pain. A series of diagnostic and laboratory tests revealed an enlarged liver and elevated alanine aminotransferase (ALT) up to 372 U/L, aspartate aminotransferase (AST) up to 99 U/L, gamma-glutamyltransferase (GGT) up to 962 U/L, and alkaline phosphatase up to 758 U/L. All potential hepatotoxic medications were discontinued. Within one week after stopping venlafaxine, her liver function test results showed marked improvement. Almost 4 weeks after discontinuing therapy, venlafaxine 37.5 mg was reinitiated. Her ALT, AST, GGT, and alkaline phosphatase again increased to 269, 49, 256, and 263 U/L, respectively, 6 days after resuming therapy. Upon discontinuation of venlafaxine, her liver function abnormalities resolved. DISCUSSION: This case is significant due to the severity of symptoms and consequent liver function test results involved in diagnosing drug-induced hepatitis. It is also remarkable because of the hepatotoxicity that occurred initially and on rechallenge with low-dose venlafaxine. The hepatotoxic effects of venlafaxine have been characterized as rare and idiosyncratic. The Naranjo probability scale revealed that the adverse drug event was probable. CONCLUSIONS: Venlafaxine therapy can lead to drug-induced hepatitis, even when used at low doses. Clinicians should be aware of this possible adverse effect of venlafaxine therapy and monitor patients closely after initiation of therapy.

Chemical and Drug Induced Liver Injury↗
PubMed1978

Effect of topical prostaglandins on nasal patency in man.

The effect of prostaglandin E1 and 17 phenyl trinor PGE2 on nasal patency has been studied in healthy volunteers and in patients with vasomotor and allergic rhinitis. Both drugs applied topically increased nasal patency. The effect of a single dose of either compound lasted for several hours. Prostaglandin E1 produced nasal irritation and throbbing, lacrimation, headache and sore throat. Except for occasional brief nasal irritation, these side effects were not encountered with 17 phenyl trinor PGE2.

Clinical Trials as Topic↗
PubMed1996

Activation of GABAB receptors increases a potassium conductance in rat bulbospinal neurons of the C1 area.

In anesthetized rats, iontophoresis of the gamma-aminobutyric acid (GABAB)-receptor agonist and antispastic drug baclofen inhibits the bulbospinal vasomotor neurons of the rostral ventrolateral medulla (RVLM). The present study was carried out to determine whether C1 adrenergic and other bulbospinal neurons of the RVLM have postsynaptic GABAB receptors. Retrogradely labeled RVLM bulbospinal neurons (n = 52) were recorded in 120-micron-thick slices from neonatal rat brain (3-10 days old). Most neurons (48/52) were tonically active (3 +/- 0.6 spikes/s). Twenty-six neurons were recovered histologically, and 18 of them were immunoreactive for tyrosine hydroxylase (TH). In current clamp, baclofen (0.3-10 microM) hyperpolarized RVLM bulbospinal cells in a dose-dependent manner (16 +/- 0.5 mV hyperpolarization by 3 microM baclofen; n = 19) and decreased input resistance by 40% (n = 10). In voltage clamp (1 microM tetrodotoxin present; holding potential: -40 to -60 mV), 3 microM baclofen induced an outward current of 21 +/- 2 pA (n = 29). This current exhibited inward rectification and reversed polarity close to the K+ equilibrium potential (external K+ from 2.5 to 10 mM). The current induced by baclofen was reduced 90% by 0.1-0.2 mM BaCl2 (n = 6) and was blocked reversibly by the selective GABAB-receptor antagonist CGP-55845A (0.5-1 microM; n = 6). All histologically verified TH-immunoreactive cells (n = 18) were sensitive to baclofen. In summary, RVLM bulbospinal neurons including C1 adrenergic cells possess GABAB receptors. Activation of these receptors increases an inwardly rectifying K+ conductance. This effect reduces the intrinsic firing frequency of RVLM vasomotor neurons "in vitro" and may contribute to the sympatholytic action of baclofen "in vivo."

Action Potentials↗
PubMed1975

Central cholinergic control of cerebral blood flow in the baboon. Effect of cholinesterase inhibition with neostigmine on autoregulation and CO2 responsiveness.

Cerebral autoregulation and vastomotor responsiveness to carbon dioxide (CO2) were measured quantitatively by the use of the autoregulation index and chemical index, respectively, in normal baboons before and after intravertebral and intracarotid infusion of the anticholinesterase agent, neostigmine methylsufate (Prostigmin). Continuous measurements were made of cerebral blood flow (measured as bilateral internal jugular venous outflow), arterial and cerebral venous pO2 and pCO2, cerebral arteriovenous oxygen differences, and endotracheal CO2. The effect of intravertebral infusion of neostigmine (12.5 mug/kg body weight) was compared to intravertebral infusion of neostigmine (25 mug/kg body weight) for assessment of any specific action of the drug on a hypothetical cholinergic vasomotor center, presumed to be located in the territory of the vertebrobasilar supply. No significant or persistent changes in cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2) followed either intravertebral or intracarotid infusion of neostigmine. Cerebral vascular resistance (CVR) and cerebral perfusion pressure (CPP), however, decreased significantly after intravertebral infusion. Cerebral autoregulatory vasoconstriction during increases of CCP was significantly reduced following both intravertebral and intracarotid infusion. Cerebral autoregulatory vasodilatation was not altered as CPP was lowered. Cerebral vasodilatory reactivity to CO2 inhalation was significantly enhanced following intravertebral neostigime but not following intracarotid neostigmine. Cerebral vasoconstrictive response to hyperventilation was not influenced by neostigmine. These results support the view that central cholinergic cerebrovascular influences exist, and are vasodilatory in nature.

Acetylcholine↗
PubMed1975

Autoperfused multi-organ preparations. II. Microcirculation in the autoperfused organs.

The microcirculation of 46 autoperfused heart-lung-liver-duodenum-pancreas-kidney preparations has been studied and the acid-base conditions were determined. The stability of the autoperfused organ preparation was not ensured by the "multi-organ" arrangement, moreover the combination had a detrimental effect, with reduced tissue perfusion leading to hypoxia and acidosis. This general vasomotor breakdown represented a therapeutic drug resistance, so that the organ preparation failed to solve the problem of temporary organ preservation.

Animals↗
PubMed1980

[Beta blockers and disturbances of the microcirculation (author's transl)].

Study of 192 cases of hypertensive patients, 89 of whom were treated by diet, general advice and correction of risk factors for an average period of 8 months. The group of patients treated beta blockers consisted of 103 subjects, 28 of whom received Propranolol, 29 Oxyprenolol, 20 Atenolol and 26 Practolol. The prevalence of Raynaud's phenomenon was markedly greater in the patients treated with beta blockers, in comparison with the group not receiving any drugs. The highest incidence of vasomotor problems was seen in the group of subjects treated with Propranolol, with 57% of patients having a Raynaud-type paroxysmal acrosyndrome. In more than half of the cases attributed to Propranolol, the clinical picture of Raynaud's syndrome was severe. Discussion of the mode of action of beta blockers on the microcirculation.

Adrenergic beta-Antagonists↗
PubMed2003

[The role of raloxifene (Evista) in the treatment and prevention of postmenopausal osteoporosis].

According to epidemiological studies in Croatia 250,000 women suffer from osteoporosis and 400,000 have osteopenia. Since osteoporosis is a disease of the elderly, and the number of older people continues to grow, it is expected that this disease and its complications (fractures) will soon become an epidemiological problem. Antiresorptive drugs include raloxifene (Evista). Raloxifene is recommended for the treatment and prevention of osteoporosis in postmenopausal women, without vasomotor symptoms. Before selection of an antiresorptive drug it is important to know not only its bone efficacy, but also other possible favorable influences on the organism. Raloxifene has positive effect on BMD (Bone Mineral Density) and bone quality. It has proven efficacy in osteoporotic fracture prevention. It is also important to emphasize the positive effect of raloxifene on the cardiovascular system and its protective effect on the breast. Raloxifene is well tolerable and is easy to take (one tablet daily, with or without food). Numerous scientific articles point to the many benefits of raloxifene. Here we would like to present the results from a randomised clinical study entitled MORE (Multiple Outcomes of Raloxifene Evaluation) conducted on 7700 postmenopausal women.

Bone Density↗
PubMed1989

Interference of prenatal and postnatal exposure to Ca2+-antagonist agents on rat functional development of vascular system.

Exposure to drugs during pregnancy can alter functional development of the vascular system. The present investigation was carried out in order to evaluate the effects of prenatal and postnatal exposure to Ca2+-antagonist (diltiazem, verapamil, and nimodipine) drugs on the development of rat vasomotor reactivity. Studies were carried out on pregnant female albino rats exposed from the first day of pregnancy until weaning to diltiazem and verapamil (6 and 24 mg/kg in their drinking water ad libitum) and nimodipine (3 and 12 mg/kg in their food ad libitum). After weaning, pups were exposed until the 60th day of age to the same treatment as their mothers were. Afterwards, pups from the 60th to 90th day of age were fed with a normal diet. In 30-, 60-, and 90-day-old conscious and anaesthetized pups, we evaluated the following: 1) systolic arterial blood pressure; 2) vasomotor responses elicited by various agents: L-noradrenaline (0.1, 1, and 5 micrograms/kg IV), L-isoprenaline (0.01, 0.1, and 1 micrograms/kg IV), and acetylcholine (0.01, 0.1, and 1 micrograms/kg IV) and by sinus-carotid baroreceptor stimulation; and 3) catecholamine, acetylcholinesterase, and adenosinase plasma levels. Prenatal and postnatal exposure to Ca2+-antagonist drugs significantly (P less than .05) decreased the pressor response to sinus-carotid baroreceptor stimulation and to L-noradrenaline and increased the hypotensive responses to L-isoprenaline and acetylcholine. Moreover, this type of treatment, although it induced a significant (P less than .05) decrease of catecholamine plasma levels, did not modify the acetylcholinesterase and adenosinase plasma levels in 30- and 60-day-old rats. On the 90th day of age, the evaluated parameters were not different from those of control rats. Our results showed that exposure to Ca2+ antagonists during pregnancy and the postnatal period may alter the functional development of rat vasomotor reactivity.

Acetylcholinesterase↗
PubMedDate not supplied

[Effect of histamine and nicotine on carbohydrate metabolic indices and the catecholamine balance in the vascular wall].

In experiments on cats subject to study was the effect of histamine and nicotine used in different doses on the level of "key" metabolites of the carbohydrate metabolism and on the catecholamines balance in the wall of vessels of different functional purpose at the instant of the maximum, bioelectric and motor response to a vasomotor agent. It was shown that the vasodilation phase observed after introduction of the mediatory type drugs was attended by activation of the carbohydrate metabolism this proving the energy-dependence of the relaxation process. The presence of variously oriented and differently marked changes in the content of the carbohydrate metabolites in vessels vessels of diverse functional purpose made it possible to classify the vessels according to the type of metabolism, which coincides with their functional purpose.

Animals↗
PubMed1995

Diagnosing vascular causes of renal failure.

The incidence of renal failure due to vascular diseases is increasing. Two reasons for this are the epidemic of atherosclerotic vascular disease in the aging population and the widespread use of vasoactive drugs that can adversely affect renal function. These vascular causes of renal failure include vasomotor disorders such as that associated with nonsteroidal antiinflammatory drugs, small-vessel diseases such as cholesterol crystal embolization, and large-vessel diseases such as renal artery stenosis. These causes of azotemia are less familiar to physicians than more classic causes, such as acute tubular necrosis, and are less likely to be recognized in their early stages. This article describes the various vascular diseases that impair renal function and outlines the steps necessary to identify them. Although some of these conditions, such as renal artery stenosis, can gradually impair function, the vascular causes of acute renal failure are emphasized in this article. Because the vasculitides primarily cause renal failure through secondary glomerulonephritis, they are mentioned only briefly. Extensive testing is rarely necessary because the cause is usually suspected through syndrome recognition. The diagnosis can then be confirmed by the results of one or two additional tests or by improved renal function after treatment.

Acute Kidney Injury↗